Using intracellular microelectrode techniques, we are able to voltage clamp selectively either the apical or the basolateral membrane of toad urinary bladder cells to any desired voltage (by passing transepithelial current). Using this technique in the presence and absence of an inhibitor of sodium transport, amiloride, we can determine the current-voltage relationship of the sodium pathway of either membrane. With this technique, it is also possible to change conditions of transport abruptly by the addition of the inhibitor or by changes in sodium concentration, and determine changes in the non-clamped membrane as a function of time. Results have indicated that the apical membrane resistance changes passively as transport is altered in a tissue whose basolateral membrane is clamped at any desired voltage. On the other hand, if the apical membrane is clamped, the basolateral membrane resistance changes abruptly as a function of transport changes, and its potential also changes in a way which indicates that there is an electrogenic component to the sodium transport system. It would appear that the mechanisms which couple the basolateral and apical membrane potentials under conditions in which transport is rapidly altered, would depend upon the sodium content of the cellular pool, and that the basolateral membrane responds extremely rapidly to such changes. In addition, we have been injecting sodium or potassium into the cells, and following the changes in membrane potential as a consequence of these injections. Results to date indicate that the basolateral membrane hyperpolarizes following sodium addition, and this is best interpreted as the turning on of an electrogenic sodium pump. We plan to inject calcium and tetramethylammonium ions in order to determine the relative effects of these substances on potassium and sodium conductance of the basolateral and apical membranes.